What Is Your Neurologic Diagnosis?

Montana M. DiVita 1Carolina Veterinary Specialists, Winston Salem, NC 27103.

Search for other papers by Montana M. DiVita in
Current site
Google Scholar
PubMed
Close
 DVM
,
Kathryn Y. Bray 1Carolina Veterinary Specialists, Winston Salem, NC 27103.

Search for other papers by Kathryn Y. Bray in
Current site
Google Scholar
PubMed
Close
 DVM
,
Lindsay M. Williams 1Carolina Veterinary Specialists, Winston Salem, NC 27103.

Search for other papers by Lindsay M. Williams in
Current site
Google Scholar
PubMed
Close
 DVM
, and
Ryan P. Traslavina 2Antech Diagnostics, Kent, WA 98032.

Search for other papers by Ryan P. Traslavina in
Current site
Google Scholar
PubMed
Close
 DVM

Click on author name to view affiliation information

A 13-year-old 39-kg (85.8-lb) castrated male Labrador Retriever was referred for evaluation of progressive pelvic limb paresis and proprioceptive ataxia of < 1 week's duration. The owners reported that the dog had a long-term history of trouble navigating stairs and jumping onto furniture, but there was a sudden onset of right pelvic limb knuckling and paraparesis 4 days prior to the evaluation. Lateral and ventrodorsal radiography of the lumbar portion of the vertebral column was performed by the referring veterinarian; radiographic findings included multifocal ventral spondylosis deformans but were otherwise unremarkable. The dog was treated with rest, tramadol (2.56 mg/kg [1.16 mg/lb], PO, q 12 h), and meloxicam (0.19 mg/kg [0.09 mg/lb], PO, q 24 h), but there was no improvement in clinical signs. The dog also had a history of chronic kidney disease that was managed with a veterinary prescription diet and laryngeal paralysis, which was not treated.

What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.

Assessment Anatomic diagnosis

ProblemRule out location
ParaparesisT3-L3 myelopathy or L4-S3 myelopathy
Proprioceptive ataxia with right pelvic limb proprioceptive deficitRight-sided T3-L3 myelopathy

Likely location of 1 lesion

Right T3-L3 spinal cord segments

Etiologic diagnosis—Primary differential diagnoses for acute lateralized progressive paraparesis and proprioceptive ataxia in a geriatric dog included neoplasia (primary or metastatic) or intervertebral disk disease (Hansen type I disk extrusion or Hansen type II disk protrusion). Less likely differential diagnoses included fibrocartilaginous embolism, infectious or noninfectious meningomyelitis, or trauma. Given the dog's age, breed, and history of laryngeal paralysis, additional considerations included metabolic or degenerative neuropathy, such as hypothyroid neuropathy or laryngeal paralysis polyneuropathy complex, respectively. These diagnoses would have been more consistent with an L4-S3 spinal cord lesion, which was initially considered a rule out location but would be unlikely to result in sudden clinical deterioration.

In addition to survey radiography, the primary veterinarian performed a CBC and serum biochemical analysis prior to the referral evaluation. The diagnostic plan included preanesthetic thoracic radiography, MRI of the thoracolumbar portion of the dog's vertebral column, and analysis of a CSF sample if warranted on the basis of MRI findings.

Diagnostic test findings—Survey thoracic radiographs were unremarkable. Magnetic resonance images were obtained with a 1.5T MRI unit.a Multiplanar T2-weighted, short tau inversion recovery (STIR), pre- and postcontrast (gadolinium) T1-weighted, and myelo-half Fourier acquisition single-shot turbo spin echo images of the thoracolumbar portion of the vertebral column were acquired. A well-defined ovoid mass causing marked (≤ 50%) right-sided spinal cord compression was present at the level of the L2-3 intervertebral disk space (Figure 1). On parasagittal sequences, there was an appearance of a golf-tee sign, suggestive of an intradural-extramedullary location of the mass. This finding was not present on the myelo-half Fourier acquisition single-shot turbo spin echo sequences. Therefore, an extradural location was not ruled out. Compared with the spinal cord, the mass was uniformly hyperintense on STIR images, slightly hyperintense on T2-weighted images, and isointense on T1-weighted images. The mass did not enhance following contrast medium administration. Given the MRI findings, primary differential diagnoses for this mass lesion included a synovial cyst or neoplasia, such as a meningioma, lymphoma, or peripheral nerve sheath tumor. A standard right hemilaminectomy was performed at the level of the L2 and L3 vertebrae. The mass was identified extradurally over the L2-3 disk space and was uniformly encapsulated. On incision of the mass, a large amount of gritty, white material along with a fibrous capsule was easily removed from the ventral and lateral aspects of the vertebral canal. On histologic examination, the tissue was found to consist of disorganized necrotic islands of fibrocartilage and hyaline cartilage separated by large amounts of hemorrhage, fibrin, and necrotic cellular debris. Additionally, areas of the tissue that were described as loosely arranged, lightly basophilic myxomatous material containing clustered and single chondrocytes and as hyalinized collagenous material containing plump mesenchymal cells were consistent with remnants of the nucleus pulposus and annulus fibrosis, respectively. The final diagnosis was necrotic nucleus pulposus with herniation, hemorrhage, and fibrosis consistent with Hansen type I intervertebral disk extrusion.

Figure 1—
Figure 1—

Right parasagittal T2-weighted (A), dorsal short tau inversion recovery (STIR; B), myelo-half Fourier acquisition single-shot turbo spin echo (HASTE; C), transverse T2-weighted (D), and transverse STIR (E) images of a 13-year-old castrated male Labrador Retriever with progressive paraparesis and pelvic limb proprioceptive ataxia. Notice a well-defined right-sided lesion at the level of the L2-3 disk space that has resulted in severe ventral and lateral spinal cord compression (A, B, and D). Compared with the gray matter of the spinal cord, the lesion is slightly hyperintense on T2-weighted images (A and D) and uniformly hyperintense on STIR sequences (B and E). The lesion has caused focal dorsal and ventral attenuation of signal from the subarachnoid space over the L2-3 disk space on myelo-HASTE images (E). A golf tee sign is apparent on T2-weighted images (A) but was not repeatable on myelo-HASTE sequences (C).

Citation: Journal of the American Veterinary Medical Association 256, 9; 10.2460/javma.256.9.981

Comments

Hansen type I disk disease is a common neurologic disorder that affects young to middle-aged chondrodystrophic dogs. Among affected dogs, type I disk disease (disk extrusion) can cause severe neurologic deficits and have considerable impact on quality of life. Specifically, chondroid degeneration of the nucleus pulposus occurs and a tear in the annulus fibrosis allows extrusion of the nucleus pulposus into the vertebral canal. Signs are usually sudden in onset because the disk material does not extrude until a tear occurs.1 In contrast, type II disk disease is characterized by fibrous degeneration of the annulus fibrosis, which thickens over time and protrudes into the spinal canal. Type II disk disease (disk protrusion) is more common in older, large-breed dogs with a long-term history of progressive signs of pain or neurologic deficits. For the dog of the present report, the signalment was not classic for Hansen type I disk disease; however, Hansen type I disk disease in many nonchondrodystrophic medium- to large-breed dogs has been described.2

The MRI features associated with Hansen type I disk disease include single-site disk herniation with dispersion of disk material cranial or caudal to the disk space.3 Ordinarily, extruded disk material has decreased MRI signal intensity because of mineralization, whereas the spinal cord often appears hyperintense as a result of concussive injury following disk extrusion.4 Contrast enhancement of compressive disk material is also seen more often in dogs with Hansen type I disk disease than it is in dogs with Hansen type II disk disease.5 For the dog of the present report, MRI findings included distinct demarcation of the lesion; the lesion was hyperintense (compared with the spinal cord) on T2-weighted and STIR images and did not enhance after contrast medium administration. The technique of STIR sequencing highlights tissue with a high water content while nulling the signal from fat; it has not been used to evaluate disk disease, to our knowledge, but is routinely used to identify paraspinal pathological changes.6 The MRI findings for the dog of the present report were more suggestive of discrete neoplasia, although a specific differential diagnosis for the uniformity of STIR hyperintensity and the lack of contrast enhancement was not readily available.

Despite the dog's nonconformity with the chondrodystrophic breeds typically affected by Hansen type I disk disease, the case described in the present report is a reminder for clinicians to carefully consider all differential diagnoses for dogs with a sudden onset of limb knuckling and paraparesis. The dog recovered following surgery and was markedly improved at the 1-month postoperative evaluation. If surgical exploration and histologic examination of the mass had not been performed, the dog's clinical history and MRI findings would have been considered highly suggestive of spinal neoplasia, which would have been associated with a guarded long-term prognosis. Further studies are needed to confirm the true incidence of Hansen type I disk disease in geriatric, large-breed dogs; nevertheless, Hansen type I disk disease should be considered a valid differential diagnosis in cases similar to that described in the present report.

Footnotes

a.

1.5T Signa LX Echo Speed Mobile MRI, General Electric, Chicago, Ill.

References

  • 1. Jeffery ND, Levine JM, Olby NJ, et al. Intervertebral disc degeneration in dogs: consequences, diagnosis, treatment, and future directions. J Vet Intern Med 2013;27:13181333.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Cudia SP, Duval JM. Thoracolumbar intervertebral disc disease in large, nonchondrodystrophic dogs; a retrospective study. J Am Anim Hosp Assoc 1997;33:456460.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Gomes SA, Volk HA, Packer RMA, et al. Clinical and magnetic resonance imaging characteristics of thoracolumbar intervertebral disk extrusions and protrusions in large breed dogs. Vet Radiol Ultrasound 2016;57:417426.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Besalti O, Peckan Z, Sirin S, et al. Magnetic resonance imaging findings in dogs with thoracolumbar intervertebral disk disease: 69 cases (1997-2005). J Am Vet Med Assoc 2006;228:902908.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Suran JN, Durham A, Mai W, et al. Contrast enhancement of extradural compressive material on magnetic resonance imaging. Vet Radiol Ultrasound 2011;52:1016.

    • Search Google Scholar
    • Export Citation
  • 6. Dennis R. Optimal magnetic resonance imaging of the spine. Vet Radiol Ultrasound 2011;52:S72S80.

All Time Past Year Past 30 Days
Abstract Views 147 0 0
Full Text Views 842 723 339
PDF Downloads 279 125 12
Advertisement